Mutants in the maize defective kernel1 (dek1) gene are blocked in embryogenesis and the endosperm is chalky and lacks an aleurone layer. Here we show that intermediate alleles result in embryos that lack a shoot axis while weak alleles result in endosperms with mosaic aleurone and deformed plants with epidermal cells that resemble bulliform cells, a specialized epidermal cell type. This indicates that dek1 functions in embryonic pattern formation, cell fate specification and pattern formation in the leaf epidermis, and cell fate specification in the endosperm. Thus, the dek1 gene product appears to control different cellular-developmental processes depending on cellular context. The phenotype of the weak dek1-Dooner allele resembles the crinkly4 (cr4) mutant phenotype. Double mutants between dek1 and cr4 showed elements of epistasis, additivity and synergy, suggesting that the gene products may function in overlapping developmental processes. cr4 transcript was detectable in dek1 mutant kernels indicating that DEK1 was not required for Cr4 transcript accumulation. To test whether DEK1 regulated the ligand for the CR4 receptor kinase, a genetic mosaic analysis was performed. The dek1 phenotype appeared to be generally cell-autonomous, leading to the conclusion that it was not likely to produce a diffusible signal molecule, and therefore was not likely to regulate the CR4 ligand.